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CVS- Cardiovascular > S2: Circulation - Vascular Smooth Muscle > Flashcards

S2: Circulation - Vascular Smooth Muscle Flashcards

1
Q

What layer in blood vessel wall are vascular smooth muscle cells mostly found?

A

Media

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2
Q

What is vascular tone?

A

It describes the degree of constriction of a blood vessel relative to maximum dilation

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3
Q

What controls vascular tone?

Why is regulating vascular tone important?

A

Vascular tone is controlled by contractile state of vascular smooth muscle cells (VSMCs). Vascular tone is present in all vessels containing VSMCs - arteries, arterioles and veins. Capillaries do not contain VSMCs so they do not have vascular tone.

Regulating vascular tone is a important target in treating cardiovascular disease

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4
Q

Difference between constrictor and dilator responses at vessel

A

Constrictor responses: act directly at VSMCs

Dilator responses: indirectly via endothelium

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5
Q

Name factors affecting constriction and dilation in lumen, endothelium and adventitia

A

In the lumen (blood stream): hormones, platelets releasing thromboxane a vasoconstrictor, immune cells releasing inflammatory mediators such as histamine, stretch

In the endothelium: Mainly produces dilators and some constrictors e.g. ET-1 –> Affect smooth muscle lying next to it

In the adventitia: Nerves

Other cells: Produce factors that affect blood flow through affecting vascular smooth muscle and tone e.g. Adenosine, K+, H+

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6
Q

Describe intrinsic or local control of vascular tone

A
  • This is the role of endothelium, immune cells, platelets, stretch
  • This regulates local blood flow to organs/tissues
  • They are important e.g. in regional hyperaemia (regional areas increase in blood flow according to need) and excersize, cold enviroment
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7
Q

Describe extrinsic and external controls

A
  • Nerves (vasoconstrictors - NA, vasodilators - Ach, NO)
  • Hormones (vasocontrictors- A, Ang II, ADH, vasodilators - ANP)
  • Feedback to the brain to make sure the body is working as a whole
  • Regulate TPR to control blood pressure which is the drive for blood flow
  • Brain function selectively alters blood flow to organs according to need e.g. during excersize, thermoregulation
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8
Q

Describe the sympathetic nerve innervation of vascular tone

A

The RVLM receives information from the CVLM and hypothalamus. The RVLM is in the brain stem and it contains the pre-sympathetic neurone that travel down the spinal cord to the thoracic spinal cord level into the intermediolateral area of spinal cord. This gives rise to preganglionic neurones. Noradrenaline/Adrenaline are the neurotransmitters used to act at adrenoreceptors to produce vasoconstriction/vasodilation.
-These nerves have bulges called varicosities where noradrenaline is released at VSM. ATP is also released.

  • Sympathetic nerve activity is tonic (1ap/s). This sets vascular tone so a fall in ongoing sympathetic activity causes vasodilation.
  • Decrease in mechanisms coupling sympathetic activity to vascular tone is an important principle in pharmacological treatment of cardiovascular disease e.g hypertension
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9
Q

List what the sympathetic NS does to the post and presynaptic membrane of synapses

A

Post-synaptic membrane:
a1 - contraction
a2- contraction (important in skin)
B2 - relaxation

Pre-synaptic membrane:
AT1 - increase release of NA (RAAS ­ sym activity)

a2- reduce release of NA (-ve feedback mechanism)
K+, adenosine etc. - reduce release of NA - important vasodilatation pathway+

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10
Q

Roles of sympathetic vasoconstrictor nerves

A
  • Contact resistance arterioles - they produce vascular tone affecting TPR and BF
  • District RVLM neurones - sympathetic pathways innervate different issues so there is modulation of particular vascular beds. e.g. during excersize which there is increased sympathetic nerve stimulation to GI (less blood flow) but reduced nerve stimulation to skin (increasing blood flow to surface so it can cool down)
  • Precapillary vasoconstriction of arterioles so less blood in given time enters capillary. Decrease in capillary pressure due to pressure drop increases absorption of interstitial fluid into blood plasma to maintain blood volume e.g. during hypovolemia
  • Control TPR -Maintains arterial blood pressure and blood flow to brain/myocardium
  • Control venous blood volume - venoconstriction causes increased venous return and increased stretch of heart, increased preload and ultimately increased SV via starlings law.
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11
Q

List hormones that control VSMC

A

Vasoconstrictors - Often upregulated
Adrenaline
Angiotensin II (Ang II)
Anti-Diuretic Hormone (ADH)

Vasodilators
Atrial natriuretic peptide (ANP)

Others
Insulin
Oestrogen
Relaxin

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12
Q

Roles of hormonal control of VSMCs

A
  1. Physiology
    Control appropriate blood flow/blood pressure during activity (exercise, standing) and maintain blood flow/blood pressure to essential organs (brain and heart) during haemodynamic crisis (haemorrhage, dehydration)
    1. Pathology
      Excess production of these agents often associated with excess vasoconstriction and vascular diseases - hypertension, heart failure
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13
Q

Name 5 important vasoconstrictor hormones

A
  1. Adrenaline
  2. Angiotensin (Ang II)
  3. ADH
  4. Endothelin-1 (ET1)
  5. Thromboxane (TXA2)
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14
Q

How is adrenaline released and what does it act on?

A
  • Released due to sympathetic nerve stimulation
  • Mainly from adrenal glands
  • At high concentrations act on a1-adrenoreceptors on VSMCs, at normal concentration act at B1 receptors
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15
Q

How is angiotensin II released and what does it act on?

A
  • Formed from RAAS
  • Very potent vasoconstrictor
  • Acts on AT1 receptors on AT1 receptors on VSMCs
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16
Q

How is ADH released and what does it act on?

A
  • Released from posterior pituitary

- High concentrations acts on V1 receptors on VSMCs

17
Q

How is Endothelin-1(ET1) released and what does it act on?

A
  • Released from endothelium

- Acts on ETA receptors on VSMCs

18
Q

How is Thromboxane (TXA2) released and what does it act on?

A
  • Released from aggregating platelets
  • Acts on TP receptors on VSMCs
  • Important vasoconstriction alongside clotting process can increase occlusion
19
Q

Describe the RAAS system

A
  • The RAAS system is stimulated by low renal blood flow, sympathetic nerves B1 and low NaCl load
  • This stimulates and releases renin from the kidneys
  • Renin act at angiotensinogen which is made in the liver which makes angiotensin I
  • Ang I is converted to ang II by ACE (mainly in the lungs because all our CO goes to the lungs so if any metabolites in the blood are needed it is likely to be there)
  • Ang II is a vasoconstrictor and stimulates sympathetic nerves to release more NA which increases TPR which also increases BP
  • Ang II also acts on adrenal glands to release aldosterone which increases blood volume because it causes more rentention of salt (Na+) at the kidneys which brings in more water by osmosis. An increase in BV increases CO and increases BP.
  • Ang II does this by binding to AT1 receptors
20
Q

Where is angiotensinogen made?

A

The Liver

21
Q

Where is vasopressin made, released and what is it’s function?

A
  • Vasopressin is made in the hypothalamus and released into blood by the posterior pituitary gland where it is stored and released into the blood stream.

ADH produces vasoconstriction and increases vascular tone.

In the kidneys, ADH causes more reabsorption of water by inserting aquaporins in the collecting duct so more water is taken back into the collecting duct promoting an increase in blood volume.

At higher concentrations of ADH, it binds to V1 receptors and causes vasoconstriction during hypovolemia which increases TPR and BP.

22
Q

Describe the feedback mechanism regulating ADH (involves the heart)?

A
  • The heart senses how well its filling (stretch), if there is poor filling there is a lack of blood return to the heart and poor CO.
  • Poor Pa stops stimulating nerves and switches off NTS which is usually an inhibitory pathway and is not activated
  • This leads to the CVLM not being switched off so it activates neurones to release ADH from posterior pituitary

Loss of blood volume increase osmolarity which increases release of ADH -> negative feedback system (maintaining BV and TPR so BP stays the same).

23
Q

Explain the myogenic response of blood vessels to changes in blood pressure

A
  • Increase distension of vessel –> Constriction
  • Decreased distension of vessel –> Dilatation
  • Maintains local blood flow during changes in local blood pressures
  • Very important in renal, coronary, cerebral circulation
  • Protective mechanism – BP drops, still good flow – BP high, less flow/damage

e.g. As pressure increases, distension increases so stretch occurs which is converted into constriction which limits blood flow under increase in pressure.

24
Q

Explain the G-protein coupled pathway that occurs when vasoconstrictors increase vascular tone in VSMCs

A
  • Vasoconstrictors bind to their Gq linked receptors (a1,AT1, V1, ETA, TP)
  • Gaq/11 pathway activated
  • PIP2 is converted to DAG and IP3 by PLC
  • DAG activates PKC
  • PKC phosphorylates VGNa+ channels increasing membrane excitability causing depolarisation
  • This activates VGCCs which induces Ca2+ influx.
  • IP3 binds to IP3 receptors on SR which also releases Ca2+
  • This increase in concentration of Ca2+ causes contraction
25
Q

What causes the release of atrial natriuretic peptide (ANP) and role?

A
  • ANP is released by specialised atria myocytes
  • Secreted by increased filling pressures stimulating stretch receptors (increase stretch means increased BV)
  • ANP opposes action of other vasoconstrictor hormones
  • ANP act at NP receptors on VSMCs - Increase cGMP pathway (like NO) causing systemic vasodilation
26
Q

What are the 3 mechanisms ANP uses to reduce BP?

A
  1. Systemic vasodilatation – opposes action of NA, Adr, Ang II, ADH, ET-1, TXA2
  2. Dilation of renal afferent arteriole - ­ Increase glomerular filtration rate ­increase Na+ and H2O excretion by the kidney - decrease blood volume ­increase urine
  3. Decrease release and actions - aldosterone, renin, ADH
27
Q

What is raised ANP a sign of?

A

Biomarker for poor heart function/congested circulation – e.g. heart failure.

CVS- Cardiovascular (24 decks)

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